title: [The changes in secretory function of pulmonary intravascular macrophages after challenge of lipopolysaccharide].
abstract: OBJECTIVE
  To investigate the role of pulmonary intravascular macrophages (PIMs) in the pathogenesis of acute lung injury (ALI) due to infection.
  
  
  METHODS
  Porcine pulmonary blood vessels were flushed by modified Morton method, and PIMs were isolated and cultured. The adhered PIMs were collected with adhesion method and incubated in RPMI 1640 medium. They were challenged with lipopolysaccharide (LPS, 10 mg/L). The activity of interleukin-1β (IL-1β), and contents of IL 6 and IL 8 in the culture supernatant were measured by method of thymocyte proliferation and enzyme linked immunoadsorbent assay (ELISA).
  
  
  RESULTS
  The released contents of IL-1β, IL-6 and IL-8 from PIMs were increased significantly compared with those before LPS challenge , and they peaked at 2 hours [IL-1β activity: (10 400 ± 2 389) scintillant count/min], 4 hours [IL-6 content: (0.80 ± 0.36) μg/L], and 6 hours [IL-8 content: (4.94 ± 1.19) μg/L ] after LPS challenge , and the differences were significant compared with hose before LPS challenge [IL-1β activity: (213 ± 85) scintillant count/min, IL-6 content: (0.27 ± 0.12) μg/L, IL-8 content: (1.84 ± 0.53) μg/L, all P <0.01].
  
  
  CONCLUSIONS
  Among the cytokines released from PIMs after LPS challenge , the increase in IL-1β occurred earlier in comparison with that of IL-6 and IL-8, suggesting that the former might play an important role at the early stage of ALI; on the other hand, though the increase in IL-6 and IL-8 contents occurred later than that of IL- 1β but it lasted for a longer duration, suggesting that they might be associated with the advancement of ALI. The Results also suggested that interaction of these cytokines played a more important role in the pathogenesis of ALI.
authors.affiliation: Department of Respiration, the 517th Hospital of PLA, Kelan 036301, Shanxi, China. LSL5516@163.com
authors.forename: Sheng-liang
authors.initials: SL
authors.lastname: Li
authors.forename: Zhi-hong
authors.initials: ZH
authors.lastname: Wu
authors.forename: Shu-qin
authors.initials: SQ
authors.lastname: Zhang
authors.forename: Cui-ping
authors.initials: CP
authors.lastname: Qin
authors.forename: Tao
authors.initials: T
authors.lastname: Li
authors.forename: Zheng-tang
authors.initials: ZT
authors.lastname: Chen
authors.forename: Jing-shun
authors.initials: JS
authors.lastname: Jin
authors.forename: Su-feng
authors.initials: SF
authors.lastname: MA
authors.forename: Jia
authors.initials: J
authors.lastname: Li
mesh_terms: D055371:Acute Lung Injury / Q000139:chemically induced* / Q000378:metabolism*; D000818:Animals; D002478:Cells, Cultured; D007378:Interleukins / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000009:adverse effects*; D016676:Macrophages, Alveolar / Q000378:metabolism*; D013552:Swine
chemical_list: D007378:Interleukins; D008070:Lipopolysaccharides